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Eating disorders in women


Authors: Pratap Sharan and A. Sundar
Date: July 2015
From: Indian Journal of Psychiatry(Vol. 57, Issue 6)
Publisher: Medknow Publications and Media Pvt. Ltd.
Document Type: Report
Length: 8,458 words
Lexile Measure: 1740L

Full Text:
Byline: Pratap. Sharan, A. Sundar

Eating disorders, especially anorexia nervosa and bulimia nervosa have been classically described in young females in Western
population. Recent research shows that they are also seen in developing countries including India. The classification of eating
disorders has been expanded to include recently described conditions like binge eating disorder. Eating disorders have a
multifactorial etiology. Genetic factor appear to play a major role. Recent advances in neurobiology have improved our understanding
of these conditions and may possibly help us develop more effective treatments in future. Premorbid personality appears to play an
important role, with differential predisposition for individual disorders. The role of cultural factors in the etiology of these conditions is
debated. Culture may have a pathoplastic effect leading to non-conforming presentations like the non fat-phobic form of anorexia
nervosa, which are commonly reported in developing countries. With rapid cultural transformation, the classical forms of these
conditions are being described throughout the world. Diagnostic criteria have been modified to accommodate for these myriad
presentations. Treatment of eating disorders can be quite challenging, given the dearth of established treatments and poor
motivation/ insight in these conditions. Nutritional rehabilitation and psychotherapy remains the mainstay of treatment, while
pharmacotherapy may be helpful in specific situations.

Introduction

Eating disorders are disorders of eating behaviors, associated thoughts, attitudes and emotions, and their resulting physiological
impairments. [sup][1] Eating disorders are associated with a significant burden on patients [sup][2] and their family members [sup][3]
and have among the highest mortality rate one of psychiatric disorders. [sup][4]

The eating disorders, especially anorexia nervosa and bulimia nervosa, have been classically described to occur in young females.
Although recent research has shown that the prevalence in males was previously underestimated, these disorders do have a clear
female preponderance. [sup][1] Various reasons have been ascribed for this finding, most of them being psychosocial. The
overvaluation of slimness, which is commonly seen in Western females, is considered to be an important contributory factor in the
pathogenesis of eating disorders. These disorders were found to be more common in "Western nations" and have been hypothesized
to be slowly spreading to "non-Western nations" as a result of the cultural transformation.

In this chapter, some of the recent research findings in eating disorder are discussed, with emphasis on Indian studies. As the
amount of research in this area in our country is relatively sparse, it is augmented with data from other developing countries. The
contribution of research from developing countries in understanding the concept of these disorders and the lacunae in current
research are discussed.

History

Cases of emaciation without medical causation were first reported in the late 17 [sup]th century. The term anorexia nervosa was
introduced by William Gull in 1874 to describe four cases of adolescent girls with deliberate weight loss. [sup][1] Weight phobia,
which is considered central to the concept of eating disorders was described as a feature of eating disorders, only in the 1930s.
[sup][5],[6] Hence, some (but not all [sup][7] ) authors suggest that weight concerns may be an artifact produced by cultural changes
in the 1930s, and may not be a core feature of the disorder.

Bulimia nervosa was first described by Russell in 1979 [sup][8] as an "ominous variant of anorexia nervosa." Later descriptions have
characterized bulimia nervosa as an independent disorder, with pathological eating behavior at a normal weight. Some authors
[sup][5] have hypothesized that bulimia nervosa was nonexistent before recent times, and changes in the cultural and economic
conditions, such as the rising prosperity and surplus of food, has led to the onset of disorder. Others [sup][9] have presented
historical cases with probable bulimia nervosa to suggest that the disorder may have existed but may not have been identified in
earlier times. However, Keel and Klump, [sup][10] who reviewed the historical cases systematically, suggest that these were closer to
binge eating disorder (BED); and that bulimia nervosa is probably a culture-bound syndrome of recent origin.

In the developing countries, anorexia nervosa was rarely reported till the 1970s and 1980s. [sup][11],[12],[13] But later studies have
confirmed the presence of eating disorders; some of these studies suggest that the prevalence of eating disorders may be similar to
that in the Western nations. [sup][10] However, in non-Western nations, patients often present without prominent weight concerns.
[sup][10]

Nosology

Based on similarities in psychopathology and high comorbidity, many authors have tried to classify eating disorders as subtypes of
mood, obsessive-compulsive, or psychotic disorders, etc. However, eating disorders "breed true," and do not evolve into a mood or
other disorders. [sup][1] In the International Classification of Disease 10 (ICD 10), [sup][14] eating disorders are considered
independently and classified under the broad category of "behavioral syndromes associated with physiological disturbances and
physical factors."

Anorexia nervosa and bulimia nervosa are the major eating disorders that are included in the Diagnostic and Statistical Manual of
Mental Disorders, 4 [sup]th Edition, Text Revision (DSM-IV-TR). [sup][15] In addition, ICD 10 [sup][14] includes "vomiting associated
with other psychological disturbances," "atypical anorexia nervosa," "atypical bulimia nervosa" and "overeating associated with other
psychological disturbances" under eating disorders. In DSM-IV-TR, anorexia nervosa is further subtyped into binge eating/purging
type and restricting type. Bulimia nervosa is subtyped into purging and nonpurging type. In DSM-IV-TR, BED has been included in
the appendix as a condition worthy of further study.

Studies have shown that the majority of the patients with eating disorders fit into the redundant category of eating disorder not
otherwise specified (EDNOS). [sup][16],[17] The validity of this category as a single diagnostic entity has been questioned; as it
includes subsyndromal forms of anorexia nervosa, bulimia nervosa as well as other disorders which do not fit into these categories.
ICD 10 partly circumvents this problem by including subsyndromal forms of the disorders as atypical anorexia nervosa and atypical
bulimia nervosa. Recent research is geared towards finding clinically useful and nosologically valid entities within the EDNOS group;
e.g., BED, night eating syndrome, purging syndrome, etc. Purging disorder is seen in individuals of normal weight who self-induce
vomiting or purge by laxatives in the absence of binge eating. Night eating syndrome is characterized by eating large quantities of
food in the night time associated with sleeplessness and morning anorexia.

Innovations in the nosology of eating disorders are expected from the future classificatory systems.

Inclusion of New Categories

The inclusion of BED and obesity is under active consideration of the DSM-V work group. [sup][18] But, the current evidence
suggests that obesity is a condition of heterogeneous etiology. Indeed, there is scant evidence that obesity, in general, is caused by
mental dysfunction. [sup][19]

Revisions in Core Defining Features

Amenorrhea

The inclusion of amenorrhea as a criterion for anorexia nervosa has been debated. It is considered useful because it is clear and
objective. Further, the presence of amenorrhea may also reflect important biological abnormalities that provide information about the
etiology of the illness and/or might inform the development of biological treatments. But studies have reported that there are many
patients who meet all clinical criteria for anorexia nervosa except for that of amenorrhea. Most of the differences between patients
with and without amenorrhea seem to reflect the nutritional status of the patient, rather than any core pathology. So, various authors
have advocated for the removal of amenorrhea as an essential criteria for the diagnosis of anorexia nervosa. [sup][20]

Fat Phobia/Weight Concerns

Reports from non-Western countries have shown that patients with symptoms suggestive of anorexia nervosa present with various
rationales for food refusal, apart from weight concerns. [sup][21],[22],[23] Lee is credited with characterizing this phenomenological
variant of anorexia nervosa. [sup][24] Lee et al . [sup][21] investigated the symptomatology of 70 Chinese patients with anorexia
nervosa in Hong Kong. Less than one-half of the patients were found to report fat phobia at any time during their illness. Instead,
weight loss was primarily attributed to stomach bloating, loss of appetite, fear of food, or simply eating less. The authors concluded
that "fat phobia, cross-culturally speaking, is not the raison d'etre for all cases of morbid self-starvation" and proposed "that the
identity of anorexia nervosa should be conceptualized without invoking the explanatory construct of fat phobia exclusively." A series
of five cases without weight concern has also been reported in India. [sup][22] Such patients with diminished weight concerns are
also seen in around 15-20% of eating disorders in the Western nations. [sup][25],[26],[27] It has also been seen that South Asians
living in Western countries present less frequently with fat phobia when compared with the white English population. [sup][28]
However, studies conducted to differentiate patients with and without weight concerns using the "Drive for Thinness" subscale of
Eating Disorders Inventory suggest that patients who score low on "Drive for Thinness" have less severe eating disorder pathology
[sup][24] and general psychopathology [sup][29] compared to patients with high scores. Furthermore, endorsement of a fat phobia
can emerge during treatment. [sup][30] Hence, while several theorists have advocated for a removal of the "weight concern" criterion
for diagnosing anorexia nervosa; [sup][31],[32],[33] others suggested that weight phobia is the sine quo non of anorexia nervosa and
should be retained in the future diagnostic systems. [sup][7] Based on a systematic review, Becker et al . [sup][24] state that nonfat
phobic anorexia nervosa does not meet the Robins and Guze's criteria [sup][34] for diagnostic validity, as a subtype of anorexia
nervosa. However, due to its frequent presentation in various countries, they suggest its inclusion as a common presentation of
EDNOS to enhance its clinical detection.

Clinical Features

The clinical features of eating disorders are varied and usually involve multiple body systems, though the key symptoms relate to
eating, body weight and shape. [sup][35]

Anorexia Nervosa

Numerous criteria have been proposed for the diagnosis of anorexia nervosa. Most of the criteria share the following essential
features:
*Weight loss/lack of weight gain and behaviors that are designed to produce such weight loss *A psychopathology characterized by
the relentless drive for thinness and/or a morbid fear of fatness. The essential psychopathology seems tightly linked to overvalued
beliefs, primarily the overvaluation of thinness. The drive for thinness as a psychopathological motif has been emphasized more by
Americans, beginning with Hilde Bruch, whereas the morbid fear of fatness, the phobic avoidance of normal weight, has been
emphasized more by the British [sup][1] *The medical consequences of starvation: For example endocrine dysfunction manifested as
amenorrhea in women and loss of sexual potency in men, hypothermia, bradycardia, orthostasis and severely reduced body fat
stores, etc *Anorexia nervosa is often, but not always, associated with disturbances of body image, the perception that one is
distressingly large despite obvious medical starvation. The distortion of body image is disturbing when present, but not
pathognomonic, invariable, or required for diagnosis. [sup][1]

The ICD 10 [sup][14] enlists the following criteria for the diagnosis of anorexia nervosa:

*There is weight loss or, in children, a lack of weight gain, leading to a body weight at least 15% below the normal or expected weight
for age and height *The weight loss is self-induced by avoidance of "fattening foods" *There is self-perception of being too fat, with an
intrusive dread of fatness, which leads to a self-imposed low weight threshold *A widespread endocrine disorder involving the
hypothalamic-pituitary-gonadal axis is manifested in women as amenorrhea and in men as a loss of sexual interest and potency (an
apparent exception is the persistence of vaginal bleeds in anorexic women who are on replacement hormonal therapy, most
commonly taken as a contraceptive pill) *The disorder does not meet the criteria A and B for bulimia nervosa.

Bulimia nervosa

The ICD 10 [sup][14] enlists the following criteria for bulimia nervosa:

*There are recurrent episodes of overeating (at least twice a week over a period of 3-month) in which large amounts of food are
consumed in short periods *There is a persistent preoccupation with eating and strong desire or a sense of compulsion to eat
(craving) *The patient attempts to counteract the "fattening" effects of food by one or more of the following: *Self-induced vomiting
*Self-induced purging *Alternating periods of starvation *Use of drugs such as appetite suppressants, thyroid preparations, or
diuretics; when bulimia occurs in diabetic patients, they may choose to neglect their insulin treatment. *There is self-perception of
being too fat, with an intrusive dread of fatness (usually leading to underweight).

Patients with bulimia nervosa have a powerful and intractable urge to overeat and have a feeling of lack of control over the episodes
of binge eating. There are controversies as regard to the criteria for what constitutes a binge. Some focus on the quantity of food
taken, some on the subjective state of the person and others on the rapid rate of eating. The DSM-IV [sup][15] gives the criterion
"eating, in a discrete period of time (e.g., within a 2-h period), an amount larger than most people would eat during a similar period
and similar circumstances" and a sense of lack of control. The clinical features of bulimia nervosa are similar to that of binge
eating/purging type of anorexia nervosa. These disorders can be differentiated by the presence of large amount of weight loss seen
in patients of anorexia nervosa.

Binge Eating Disorder

BED is characterized by recurrent episodes of binge eating in the absence of regular compensatory behavior such as vomiting or
laxative abuse. Related features include eating until uncomfortably full, eating when not physically hungry, eating alone and feelings
of depression or guilt. Although it is not limited to obese individuals, it is most common in this group and those who seek help do so
for treatment of overweight rather than for binge eating. The prevalence of BED is reported to be 2-5% in community samples, and
30% in individuals who seek weight control treatment. It has a more equal gender ratio than bulimia nervosa. [sup][36] BED eating
disorder is associated with increased psychopathology including depression and personality disorders.

Comorbidity

The diagnostic challenges of eating disorders are only partly addressed when a specific eating disorder is identified, because, in the
large majority of cases, comorbid psychiatric disorders accompany the eating disorder. [sup][1] Common co-occurring conditions
include:

Mood/affective disorders

Affective disorders are commonly seen in patients with both anorexia and bulimia nervosa. [sup][35] Recent studies have shown a
high degree of comorbidity between bipolar affective disorders and eating disorders, especially between bulimia nervosa and bipolar
II disorders. [sup][37] This comorbidity becomes more apparent when subthreshold forms of the disorders are included. [sup][38]

Anxiety disorders

The prevalence of anxiety disorders in general and obsessive compulsive disorder, in particular, is much higher in people with
anorexia and bulimia nervosa. Anxiety disorders often have their onset in childhood before the onset of an eating disorder, supporting
the possibility they are a vulnerability factor for developing anorexia nervosa or bulimia nervosa. [sup][39]

Substance use disorders

Eating disorders are associated with increased risk of multiple substance use disorders, with the risk being more for bulimia nervosa
and binge eating/purging subtype of anorexia nervosa. [sup][40],[41]

Personality traits and disorders

It has been suggested that anorexia nervosa may be associated with obsessional and perfectionistic forms of personality
disturbances, bulimia nervosa with impulsive and unstable personality disorders, and BED with avoidant and anxious forms of
personality disorders. [sup][42] Cluster B and obsessive-compulsive personality disorders have been reported to predict a poorer
course and/or outcome, and histrionic personality traits and self-directedness have been reported to predict a more favorable course
and/or outcome. In the setting of an eating disorder, vulnerable personality traits may be amplified into what appear to be primary
personality disorders but are actually secondary personality disturbances.

Other psychiatric disorders

There is a high comorbidity of anorexia nervosa with body dysmorphic disorder-estimated at 25-39% - in which patients additionally
have obsessional preoccupations regarding specific body parts not related to weight or shape in particular. [sup][1]

Complications and Mortality

Medical complications in eating disorders results from (a) the amount and rate of starvation, (b) the means used to produce weight
loss (dieting alone, with or without over exercising, self-induced vomiting, laxatives, diet pills, diuretics), and (c) binge eating.

In patients with anorexia nervosa, every major organ system can be involved, and the risk of mortality is substantial. Particular areas
of concern include dermatologic changes (some of which evidently need acute intervention; e.g., purpura), endocrine abnormalities
(including mismanagement of diabetes), gastrointestinal problems (including the risk of gastric dilatation), cardiovascular/pulmonary
problems (including arrhythmias and pneumomediastinum), severe electrolyte abnormalities, and bone demineralization. [sup][43]

Eating disorders are associated with one of the highest rates of mortality among psychiatric disorders up to 19% within 20 years of
onset among those initially requiring hospitalization. [sup][1] Eating disorder patients die from either the medical consequences of
starvation (cardiac muscle loss and arrhythmia, sometimes related to hypokalemia) or suicide. In a meta-analysis conducted in 1995
of 42 published studies, [sup][44] the crude mortality rate was 5.9%, translating into 0.56%/year or 5.6% per decade. In the studies
specifying the cause of death, 54% of the patients died as a result of eating disorder complications, 27% committed suicide, and the
remaining 19% died of unknown or other causes. [sup][45] In a meta-analysis of standardized mortality rates (SMR) in 2001, the
overall aggregate SMR of anorexia nervosa in studies with 6-12 years of follow-up was 9.6 and in studies with 20-40 years of follow-
up 3.7. [sup][46] Anorexia nervosa comorbid with alcohol dependence is associated with up to 50 times higher, and anorexia nervosa
comorbid with insulin-dependent diabetes mellitus with up to 10 times higher mortality than each of these illnesses alone. [sup][1]

Epidemiology

Western countries

Incidence

Most incidence studies of eating disorders have used psychiatric case registers or medical records of hospitals in circumscribed
areas. Hence they underestimate the incidence in the community. The reported incidence rates of anorexia nervosa and bulimia
nervosa are up to 8/100,000 persons/year and 13/100,000 persons/year, respectively. [sup][45] Studies, including meta-analysis in
Western cultures suggest that the incidence of anorexia nervosa increased up to the 1970s when it reached a plateau. [sup][47],[48]
On the other hand, the incidence rate of bulimia nervosa is increasing. [sup][10] Eating disorders seem to have become more
common among younger females during the latter half of the 20 [sup]th century in Western cultures, during a period when icons of
beauty (e.g., contestants at beauty contests) became thinner and women's magazines published significantly more articles on
methods for weight loss. [sup][49],[50],[51],[52]

Prevalence

Based on the National Comorbidity Survey replication, lifetime prevalence estimates of anorexia nervosa, bulimia nervosa, and BED
are 0.9%, 1.5%, and 3.5%, respectively, in women, and 0.3%, 0.5%, and 2.0% in men. [sup][53] Other researches suggest that only
about 15% of individuals have no preoccupation with dieting, weight or shape; hence, subthreshold disorders of eating behaviors may
be more prevalent. Eating disorders are among the most gender-divergent disorders in psychiatry, but the divergence is substantially
narrower than previously believed. Previous estimates of the ratio of men to women for eating disorders were typically 1 in 20-1 in 10.
Recent community-based epidemiological studies, however, found ratios of approximately 3 to 1 for both anorexia nervosa and
bulimia nervosa. [sup][1]

Non-Western countries

Earlier studies suggested that anorexia nervosa was rare in non-Western countries, including India. [sup][54],[55],[56]
Epidemiological studies in Korea have shown a prevalence rate of 0.02-0.03%. [sup][57],[58] Nakamura et al . [sup][59] found a
prevalence of 0.003% of general population, and 0.005% of female population had anorexia nervosa; and 1.02/100000 females had
bulimia nervosa in a circumscribed area in Japan. Kuboki et al . [sup][60] found a prevalence of 2.9-3.7/100,000 for eating disorders
in 1985 and 3.6-4.5/100,000 for anorexia nervosa and 1.3-2.5/100,000 for bulimia nervosa in 1992 in Japan. Azuma and Henmi
[sup][61] found a rural/urban difference with 0.2% prevalence in urban areas and 0.05% in rural areas. Chen et al . [sup][62] found a
prevalence of 0.03% in Hong Kong. Nobakht and Dezhkam [sup][63] reported a prevalence of 0.9% for anorexia nervosa and 3.2%
for bulimia nervosa among high school students in Iran. Surveys among high school students found a prevalence of 0.9% in Egypt
[sup][64] and 0.002% in Pakistan for bulimia nervosa. [sup][65] Further, authors have noted an increasing prevalence of eating
disorders associated with body dissatisfaction in non-Western countries, which is hypothesized to be the effect of Westernization.
[sup][66] Studies in Western countries show that eating disorders occur more frequently among ethnic minorities. [sup][67],[68]

Keel and Klump [sup][10] in their review of studies in non-Western countries, comment that "excluding the criterion of weight
concerns, anorexia nervosa appears to represent a similar proportion of the general and psychiatric populations in several Western
and non-Western nations." Another interesting finding reported was the relatively lower difference in prevalence of bulimia nervosa
and anorexia nervosa in non-Western countries compared to Western countries. The authors hypothesize that bulimia is more
culturally dependent than anorexia nervosa.

Etiology and Risk Factors

Currently, eating disorders are considered to be complex disorders with multifactorial etiology, involving biological, [sup][69]
psychological, and environmental factors, like most other psychiatric syndromes. [sup][1]
Biological Factors

Biological theories for eating disorders have been in vogue since late 19 [sup]th century when eating disorders were considered to
result from postpartum pituitary necrosis. Although this theory was soon disproved, a variety of subsequent theories have been
advanced focusing on putative biological underpinnings - for example, the hypothesis that some predisposing hypothalamic
abnormality exists, evidenced by amenorrhea. However, recent evidence suggests that the endocrine abnormalities occur as a
consequence of starvation. [sup][1] The current biological hypothesis suggests that eating disorders represent a distortion and
overriding of the normal neurobiologically regulated eating behaviors in response to the continued drive for thinness and a fear
conditioning about normal weight.

Recent evidence has shown a strong genetic contribution to the etiology of eating disorders. Twin studies demonstrate a 3 times
higher concordance in monozygotic twins compared to dizygotic twins. Genetic factors may contribute more than 50% to the
appearance of anorexia nervosa and bulimia nervosa. Large studies have shown consistent (but not specific) linkage between
polymorphic variants of 5-HT(2A) receptor gene and the BDNF gene and anorexia nervosa restricting subtype. [sup][70] Andersen
and Yager [sup][1] suggest that genetic factors probably contribute by increasing the presence and strength of risk factors, such as
persevering, perfectionistic, sensitive, fearful, or impulsive personality traits, or through biological vulnerabilities that more easily lead
to disrupted regulation of serotoninergic mechanisms when dieting occurs.

Contemporary theories have pointed to putative serotonin mechanisms, based on observations that individuals with anorexia nervosa
have abnormal cerebrospinal fluid serotonin levels when ill, that may not completely reverse on partial weight gain. [sup][71] Brain
imaging studies, using 5-HT specific ligands, show that disturbances of 5-HT function occur when people are ill, and persist after
recovery from anorexia nervosa and bulimia nervosa. [sup][72] It is postulated that that a trait-related disturbance of 5-HT neuronal
modulation predates the onset of anorexia nervosa and contributes to premorbid symptoms of anxiety, obsessionality, and inhibition.
[sup][72] Other neuromodulators such as disturbed corticotropin releasing hormone, opioids, cholecystokinin, neuropeptide Y, peptide
YY, leptin, ghrelin, etc., have also been implicated in the etiology of eating disorders.

Neuroimaging studies suggest that white matter and gray matter volume losses occur in eating disorders, but these remit with
recovery. Studies have implicated cingulate, frontal, temporal, and parietal regions in anorexia nervosa. Functional studies suggest
that challenges such as food and body image distortions may activate some of these regions. These disturbances persist after
recovery from anorexia nervosa, raising the possibility that these traits may be a part of the vulnerability to develop an eating
disorder. [sup][73]

Psychological Factors

In the first half of the 20 [sup]th century, psychodynamic formulations of eating disorders predominated. Early formulations were
centered on fear of oral impregnation: However, they were replaced by formulations emphasizing maturational and existential fears;
with restricting type anorexia nervosa being hypothesized as providing an escape from onrushing negative visions of the emerging
sexuality and other biological and social challenges of adolescence.

Presence in childhood of traits such as perfectionism, rigidity, and being rule-bound each increase the risk of subsequently
developing anorexia nervosa by a factor of nearly seven. Trauma during childhood or adolescence contributes to the likelihood of
later psychiatric disorders, in general, not specifically an eating disorder.

Investigators are beginning to identify endophenotypes have like poor set shifting and weak central coherence the help of family
studies. [sup][74],[75],[76] These might help in unraveling the psychobiology of eating disorders.

Environmental Factors

Keel and Klump [sup][10] have commented that culture seems to have a pathoplastic effect in anorexia nervosa with regards to
weight concern while bulimia nervosa seems to be a culture-bound syndrome. Many of the cases from non-Western countries have
been found to lack weight concerns.

The view that eating disorders are etiologically related to the internalization of the social pressure resulting from the standards of
female beauty of the modern industrial society or Western culture holds a dominant position in the current discourse around etiology
of eating disorders. [sup][77] Environmental factors like enrollment to ballet schools, teasing by family and friends, and comments and
directives from authority figures (doctors, nurses, teachers, coaches) regarding need to change weight play a role in the pathogenesis
of eating disorders.

Lee [sup][78] suggests that admiration of thinness is not inherent to non-Western cultures. Kayano et al . [sup][79] compared the
body dissatisfaction and eating attitudes among students from Indian (residing in Muscat, Oman), Omani, Filipino, Japanese and
Euro-American backgrounds. Subjects from India, Oman and the Philippines demonstrated eating attitudes that were similar to or
worse than subjects from Western countries and Japan, but their desire for thinness was not as strong. The study showed that
although non-Western cultures have disordered eating behavior, it may be motivated by reasons other than body dissatisfaction.
However globalization and exposure to Western media may increase the rate of eating disorders in non-Western countries. Recent
studies from Fiji suggest that the introduction of popular television programs highlighting slimness and stigmatizing obesity launched
widespread dieting behavior and led to the emergence of new cases of eating disorders in populations that were previously
unconcerned with these issues. [sup][80]

Westernization is not the only cultural factor playing an etiological role in eating disorders. Some studies have found an increased
prevalence of disordered eating behaviours (as measured by Eating Attitude Test scores) in ethnic minorities in Western countries;
[sup][81] and a correlation between disordered eating behavior and a "traditional" South Asian cultural orientation. It was
hypothesized that difficulties in integration into the Western society led to the disordered eating behavior. However, even this
evidence points to the importance of cultural factors in the pathogenesis of eating disorders, even as it clarifies that more than one
cultural factor may play a role.

Some cases of eating disorder are hypothesized to be a caused and maintained by family pathology. [sup][35]
Management of Eating Disorders

The core treatment goals for all eating disorders are as follows: [sup][1]

*Attaining and maintaining a normal, healthy, individualized, stable body weight; *Stopping all abnormal eating behaviors, such as
food restricting, binge eating, or purging, and associated abnormal behaviors, especially compulsive exercise; *Dismantling the core
overvalued beliefs and unhealthy cognitive "schemas" of automatic cognitive distortions, replacing them with healthy, balanced views
of self (not primarily dependent on body weight or shape) and the capacity for emotional and behavioral self-regulation; *Treating the
comorbid conditions, psychiatric and medical; and *Planning for ongoing relapse prevention for approximately 5 years after acute
improvement.

The management of eating disorders begins with forming of a therapeutic alliance, followed by a comprehensive psychiatric and
medical evaluation (including body mass index). The need for laboratory analyses should be determined on an individual basis. Bone
density examinations should be obtained for patients who have been amenorrheic for 6 months or more.

Treatment planning requires matching the intensity of treatment to the severity of illness. The decision about whether a patient should
be hospitalized on a psychiatric versus a general medical or adolescent/pediatric unit should be made based on the patient's general
medical and psychiatric status, the skills and abilities of local psychiatric and general medical staff, and the availability of suitable
programs to care for the patient's general medical and psychiatric problems.

The methods of treatment include medical, nutritional, educational, psychotherapeutic, behavioral, and pharmacological components.

Nutritional Rehabilitation

The goals of nutritional rehabilitation for seriously underweight patients are to restore weight, normalize eating patterns, achieve
normal perceptions of hunger and satiety, and correct biological and psychological sequelae of malnutrition. The initial short-term
goal is to restore patients fully, safely, and promptly to the ideal healthy range as specified in population weights for age, height, and
gender or the weight at which there is a 50% chance of return of menses for adolescent girls. Caloric intake should be carefully
tailored to avoid refeeding syndrome. Caloric intake levels should usually start at 30-40 kcal/kg/day (approximately 1000-1600
kcal/day). During the weight gain phase, intake may have to be advanced progressively to as high as 70-100 kcal/kg/day for some
patients.

Pharmacotherapy

Antidepressants, antipsychotics, anticonvulsants, prokinetic agents, opiate antagonists, appetite suppressants, tetrahydrocannabinol,
cyproheptadine, zinc, and ondansetron have been tested for the treatment of eating disorders. Available evidence shows that
fluoxetine may be beneficial in relapse prevention of anorexia nervosa after weight restoration. [sup][82] Cyproheptadine has been
shown to have some modest benefits in the weight restoration phase of anorexia nervosa treatment. [sup][83] Antidepressants,
especially selective serotonin reuptake inhibitors, at a higher dose (e.g., 60 mg of fluoxetine) may be useful in the treatment of bulimia
nervosa and BED.

Psychotherapy

Psychotherapies aimed at modifying and altering core pathological beliefs and other contributing psychopathological issues are key
elements of treatment. Available evidence strongly favors treatments based on cognitive-behavioral therapies (CBT). Patients of
anorexia nervosa without weight concern respond as well with CBT. [sup][27] Additional alternative psychotherapeutic interventions
based on interpersonal therapies, family therapies, or psychodynamically informed psychotherapies - particularly those using self-
psychology and "focal analytical" approaches - may also be beneficial. [sup][1]

Indian Studies on Eating Disorders

Jha and Awadhia [sup][84] were probably the first to report a case of eating disorder in India. They describe the case of a 42-year-old
female with self-induced starvation of 3 weeks duration with the belief that fasting would improve her memory. She was not reported
to have any weight concerns or body image disturbance. The case report did not mention the extent of weight loss and history
regarding amenorrhea. Neki et al . [sup][85] reported a pair of monozygotic twin females aged 15, who presented with the rejection of
food, loss of weight and secondary amenorrhea. These cases also lacked body image disturbances. Chadda et al . [sup][86] reported
a case of anorexia nervosa that met the DSM-III criteria in a 13-year-old female with comorbid systemic lupus erythematosus. This
patient had an onset of illness following taunts by parents and siblings regarding her steroid induced weight gain. Khandelwal et al .
[sup][22] reported a case series of 5 patients who had many features of anorexia nervosa but no body image disturbances. Following
this there have been recent reports of binge/purging type of anorexia nervosa [sup][87] and bulimia nervosa. [sup][88]

Epidemiology

Although some authors have commented that anorexia nervosa is not as rare in India as previously reported, [sup][89] no general
population study has been conducted in India. Some studies have been done in special populations, but almost all of them have
depended on self-report inventories (for case identification) or chart reviews. Bhugra and King [sup][90] have questioned the
applicability of the self-report instruments for eating attitudes in non-Western cultures, when no attempt is made to ascertain the
respondent's understanding of the often subtle and Western orientation of many questions.

Srinivasan et al . [sup][91] studied 210 medical students with standardized instruments and found that none of the students could be
diagnosed as having anorexia nervosa or bulimia nervosa. However, around 15% of students suffered from a subthreshold disorder
which they labeled "Eating Distress Syndrome."

Bhugra et al . [sup][92] conducted a study on 504 students in an all-girls private college in an industrial town in north India using the
Hindi translation of the Bulimia Investigatory Test, Edinburgh. They found that 2 patients scored above the cutoff for bulimia nervosa,
giving a prevalence of around 0.4%.
Mammen et al . [sup][93] conducted a retrospective chart review of children and adolescents (<18 years) attending the Child and
Adolescent Psychiatry Unit, Christian Medical College and Hospital, Vellore, from January 2000 to December 2005. The 6-year
period prevalence of eating disorder as per ICD 10 was 1.25%. The most common diagnosis was psychogenic vomiting (85.4%); only
six cases (14.6%) of anorexia nervosa were reported. About 43.9% of patients with eating disorder had a psychiatric comorbidity, with
common comorbid diagnoses being mood disorder (27.8%), intellectual disability (22.2%), and dissociative disorder (16.7%). This
study differed from most other studies by including psychogenic vomiting as an eating disorder.

Some studies have demonstrated that weight concerns and abnormal eating behaviors are common in Indian adolescents. Chugh
and Puri [sup][94] assessed 150 adolescents from an affluent background in Delhi. They found that 96% of obese, 88% of normal-
weight, and 42% of underweight subjects were dissatisfied with their current weight. While the majority of the obese subjects (63:3%)
wanted to lose more than 16 kg, even subjects in the normal-weight (88%) and underweight (32%) groups wanted to lose between 5
and 16 kg. The frequency of dieting was greater in obese subjects (76:6%) but was also reported in normal weight (38%) and
underweight (14%) subjects. Gupta et al . [sup][95] compared students from India and Canada and found that after the effect of body
mass index was statistically controlled, the Canadian and Indian women scored similarly on some of the core features of eating
disorders, as measured by the Drive for Thinness and Body Dissatisfaction subscales of Eating Disorder Inventory. Similarly, Rubin
et al . [sup][96] did not find any evidence of difference on body image discrepancy and eating pathology in school children from India,
France Tibet, and the United States of America. These studies suggest that eating disorders do occur in India and with increasing
level of Westernization, the prevalence may increase in future, although, further studies are needed to confirm this supposition.

Clinical Features

Khandelwal et al ., [sup][22] reported a series of 5 patients. All the patients presented with most of the symptoms of eating disorder
but lacked the disturbance of body image, drive for thinness or fear of becoming fat. But, the patients were indifferent to their loss of
weight and emaciation and rationalized their decreased food intake. The authors hypothesized that fear of fatness might be a
common but inessential feature of anorexia nervosa. Weight concern and consequent slimming may be the most frequent mode of
entry into the disorder in some cultures but not in others.

Srinivasan et al . [sup][91],[97] reported that subsyndromal forms of eating disorder are more common in the Indian population and
suggest the term "Eating Distress Syndrome" for such cases with the following criteria:

*Eating habits and body shape as a source of conflict and concern with the need to change them *Felt need for or sought
professional help *Bingeing once a week: Short lived binges associated with guilt but no counter-binge behaviors like starvation,
vomiting, purging, etc *Strict dieting, but no rigorous measures like full day starvation or use of diet pills. Slimming exercises practiced
*No significant change in body weight because of above measures.

However, this syndrome has not been studied further.

Summary of Studies Done in India

Most of the early literature on eating disorders have been in the form of case reports and chart review, which have demonstrated that
various forms of eating disorders do exists in our population. This was not followed by any population-based epidemiological study;
hence, the prevalence of these disorders in our country is currently unknown. Recent studies have shown that abnormal eating
behaviors and weight concern is common among the student population and cross-cultural studies have shown that it may be nearly
equal to that of Western nations. The clinical presentation of eating disorders in India is similar to that of other developing nations,
with the absence of weight concern in most of the reported cases. This has both diagnostic and treatment implications, as models of
psychotherapy which focus on weight concern may not be applicable in this population.

Future Directions

The study of eating disorders in developing countries like India could be illuminating, as it provides a unique opportunity for testing
the role of culture in the etiology of eating disorders. The relative rarity of eating disorders in psychiatric centers (about one case per
year) may pose a problem in this regard. [sup][89],[93] It may be possible that the bulk of patients with eating disorders, particularly if
they have somatic rather than body shape/weight concerns, may be seeking care from general physicians and
gastroenterologists/endocrinologists. Hence, chart reviews of general medical records may be able to identify "hidden" cases.

Epidemiological studies are needed to assess the burden of these diseases in our population. Indigenously designed culturally
appropriate instruments may be needed for this. It would also be interesting to study the "atypical" clinical presentation of eating
disorders in India (i.e., without weight concern). This would have widespread implications in refining the nosology and clarifying the
pathophysiology of eating disorders. There has been no research on the treatment of eating disorders in India. Given the clinical
presentation, it would be necessary to study whether usual models of psychotherapy would work, or other indigenous models would
be needed to cater to the unique needs of our population.

Conclusions

Eating disorders have long been considered as culture bound syndromes, restricted to countries with Western culture. Current
evidence shows that culture may have a formative as well as the pathoplastic effect on eating disorders. It has been hypothesized
that there may be multiple pathways of entry into eating disorder pathology, but weight concern and body dissatisfaction may be the
most common pathways, even in developing countries (through westernizing influences). Research in eating disorders in India may
be useful in understanding the pathophysiology of these disorders and for planning services (preventive and therapeutic) in the
country.

References

1. Andersen AE, Yager J. Eating disorders. In: Sadock BJ, Sadock VA, Ruiz P, editors. Kaplan and Sadock's Comprehensive
Textbook of Psychiatry. 9 [sup]th ed. Philadelphia: Lippincott Williams and Wilkins; 2009. p. 2128-49.

2. Mond J, Rodgers B, Hay P, Korten A, Owen C, Beumont P. Disability associated with community cases of commonly occurring
eating disorders. Aust N Z J Public Health 2004;28:246-51.

3. Zabala MJ, Macdonald P, Treasure J. Appraisal of caregiving burden, expressed emotion and psychological distress in families of
people with eating disorders: A systematic review. Eur Eat Disord Rev 2009;17:338-49.

4. Harris EC, Barraclough B. Excess mortality of mental disorder. Br J Psychiatry 1998;173:11-53.

5. Casper RC. On the emergence of bulimia nervosa as a syndrome. Int J Eat Disord 1983;2:3-16.

6. Russell GF. The changing nature of anorexia nervosa: An introduction to the conference. J Psychiatr Res 1985;19:101-9.

7. Habermas T. In defense of weight phobia as the central organizing motive in anorexia nervosa: Historical and cultural arguments
for a culture-sensitive psychological conception. Int J Eat Disord 1996;19:317-34.

8. Russell G. Bulimia nervosa: An ominous variant of anorexia nervosa. Psychol Med 1979;9:429-48.

9. Habremas T. The psychiatric history of anorexia nervosa and bulimia nervosa: Weight concerns and bulimic symptoms in early
case reports. Int J Eat Disord 1989;8:259-73.

10. Keel PK, Klump KL. Are eating disorders culture-bound syndromes? Implications for conceptualizing their etiology. Psychol Bull
2003;129:747-69.

11. Neki JS. Psychiatry in South-East Asia. Br J Psychiatry 1973;123:257-69.

12. Buhrich N. Frequency of presentation of anorexia nervosa in Malaysia. Aust N Z J Psychiatry 1981;15:153-5.

13. Lee S, Chiu HF, Chen CN. Anorexia nervosa in Hong Kong. Why not more in Chinese? Br J Psychiatry 1989;154:683-8.

14. World Health Organisation. The ICD-10 Classification of Mental and Behavioural Disorders. Clinical Descriptions and Diagnostic
Guidelines. Geneva: World Health Organisation; 1992.

15. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. (4 [sup]th ed., Text Rev.). Washington,
DC: American Psychiatric Association; 1994.

16. Ricca V, Mannucci E, Mezzani B, Di Bernardo M, Zucchi T, Paionni A, et al. Psychopathological and clinical features of
outpatients with an eating disorder not otherwise specified. Eat Weight Disord 2001;6:157-65.

17. Turner H, Bryant Waugh R. Eating disorder not otherwise specified (EDNOS): Profiles of clients presenting at a community eating
disorder service. Eur Eat Disord Rev 2004;12:18-26.

18. Walsh TB. Report of the DSM-V Eating Disorders Work Group November, 2008. Available from:
http://www.psych.org/MainMenu/Research/DSMIV/DSMV/DSMRevisionActivities/DSMVWorkGroupReports/EatingDisordersWorkGroupReport.aspx.
[Last accessed on 2009 Dec 04].

19. Marcus MD, Wildes JE. Obesity: Is it a mental disorder? Int J Eat Disord 2009;42:739-53.

20. Attia E, Roberto CA. Should amenorrhea be a diagnostic criterion for anorexia nervosa? Int J Eat Disord 2009;42:581-9.

21. Lee S, Ho TP, Hsu LK. Fat phobic and non-fat phobic anorexia nervosa: A comparative study of 70 Chinese patients in Hong
Kong. Psychol Med 1993;23:999-1017.

22. Khandelwal SK, Sharan P, Saxena S. Eating disorders: An Indian perspective. Int J Soc Psychiatry 1995;41:132-46.

23. Bennett D, Sharpe M, Freeman C, Carson A. Anorexia nervosa among female secondary school students in Ghana. Br J
Psychiatry 2004;185:312-7.

24. Becker AE, Thomas JJ, Pike KM. Should non-fat-phobic anorexia nervosa be included in DSM-V? Int J Eat Disord 2009;
42:620-35.

25. Ramacciotti CE, Dell'Osso L, Paoli RA, Ciapparelli A, Coli E, Kaplan AS, et al. Characteristics of eating disorder patients without
a drive for thinness. Int J Eat Disord 2002;32:206-12.

26. Strober M, Freeman R, Morrell W. Atypical anorexia nervosa: Separation from typical cases in course and outcome in a long-term
prospective study. Int J Eat Disord 1999;25:135-42.

27. Dalle Grave R, Calugi S, Marchesini G. Underweight eating disorder without over-evaluation of shape and weight: Atypical
anorexia nervosa? Int J Eat Disord 2008;41:705-12.

28. Tareen A, Hodes M, Rangel L. Non-fat-phobic anorexia nervosa in British South Asian adolescents. Int J Eat Disord 2005;
37:161-5.

29. Abbate-Daga G, Piero A, Gramaglia C, Gandione M, Fassino S. An attempt to understand the paradox of anorexia nervosa
without drive for thinness. Psychiatry Res 2007;149:215-21.

30. Soomro GM, Crisp AH, Lynch D, Tran D, Joughin N. Anorexia nervosa in 'non-white' populations. Br J Psychiatry 1995;
167:385-9.
31. Palmer RL. Weight concern should not be a necessary criterion for the eating disorders: A polemic. Int J Eat Disord 1993;
14:459-65.

32. Katzman MA, Lee S. Beyond body image: The integration of feminist and transcultural theories in the understanding of self
starvation. Int J Eat Disord 1997;22:385-94.

33. Rieger E, Touyz SW, Swain T, Beumont PJ. Cross-Cultural Research on Anorexia Nervosa: Assumptions Regarding the Role of
Body Weight. Int J Eat Disord 2001;29:205-15.

34. Robins E, Guze SB. Establishment of diagnostic validity in psychiatric illness:Its application to schizophrenia. Am J Psychiatry
1970;126:983-7.

35. Chandra PS, Chaturvedi SK, Jagdeesh AN. In: Vyas JN, Ahuja N, editors. Textbook of Postgraduate Psychiatry. 2 [sup]nd ed.
New Delhi: Jaypee Brothers Medical Publishers; 1999. p. 357-68.

36. de Zwaan M. Binge eating disorder and obesity. Int J Obes Relat Metab Disord 2001;25 Suppl 1:S51-5.

37. McElroy SL, Kotwal R, Keck PE Jr, Akiskal HS. Comorbidity of bipolar and eating disorders: Distinct or related disorders with
shared dysregulations? J Affect Disord 2005;86:107-27.

38. McElroy SL, Kotwal R, Keck PE Jr. Comorbidity of eating disorders with bipolar disorder and treatment implications. Bipolar
Disord 2006;8:686-95.

39. Kaye WH, Bulik CM, Thornton L, Barbarich N, Masters K. Comorbidity of anxiety disorders with anorexia and bulimia nervosa. Am
J Psychiatry 2004;161:2215-21.

40. Krug I, Pinheiro AP, Bulik C, Jimenez-Murcia S, Granero R, Penelo E, et al. Lifetime substance abuse, family history of alcohol
abuse/dependence and novelty seeking in eating disorders: Comparison study of eating disorder subgroups. Psychiatry Clin Neurosci
2009;63:82-7.

41. Root TL, Pinheiro AP, Thornton L, Strober M, Fernandez-Aranda F, Brandt H, et al. Substance use disorders in women with
anorexia nervosa. Int J Eat Disord 2010;43:14-21.

42. Grilo CM. Recent research of relationships among eating disorders and personality disorders. Curr Psychiatry Rep 2002;4:18-24.

43. Mitchell JE, Crow S. Medical complications of anorexia nervosa and bulimia nervosa. Curr Opin Psychiatry 2006;19:438-43.

44. Sullivan PF. Mortality in anorexia nervosa. Am J Psychiatry 1995;152:1073-4.

45. Hoek HW. Incidence, prevalence and mortality of anorexia nervosa and other eating disorders. Curr Opin Psychiatry 2006;
19:389-94.

46. Nielsen S. Epidemiology and mortality of eating disorders. Psychiatr Clin North Am 2001;24:201-14, vii.

47. Hoek HW, van Hoeken D. Review of the prevalence and incidence of eating disorders. Int J Eat Disord 2003;34:383-96.

48. Milos G, Spindler A, Schnyder U, Martz J, Hoek HW, Willi J. Incidence of severe anorexia nervosa in Switzerland: 40 years of
development. Int J Eat Disord 2004;35:250-8.

49. Garner DM, Garfinkel PE, Schwartz D, Thompson M. Cultural expectations of thinness in women. Psychol Rep 1980;47:483-91.

50. Owen PR, Laurel-Seller E. Weight and shape ideals: Thin is dangerously in. J Appl Sociol 2000;30:979-90.

51. Rubinstein S, Caballero B. Is Miss America an undernourished role model? JAMA 2000;283:1569.

52. Wiseman CV, Gray JJ, Mosimann JE, Ahrens AH. Cultural expectations of thinness: An update. Int J Eat Disord 1992;11:85-9.

53. Hudson JI, Hiripi E, Pope HG Jr, Kessler RC. The prevalence and correlates of eating disorders in the National Comorbidity
Survey Replication. Biol Psychiatry 2007;61:348-58.

54. Dube KC. A study of prevalence and biosocial variables in mental illness in a rural and an urban community in Uttar Pradesh -
India. Acta Psychiatr Scand 1970;46:327-59.

55. Nandi DN, Das NN, Chaudhuri A, Banerjee G, Datta P, Ghosh A, et al. Mental morbidity and urban life-an epidemiological study.
Indian J Psychiatry 1980;22:324-30.

56. Varghese A, Beig A. Neurosis in Vellore town-an epidemiological study. Indian J Psychiatry 1974;16:1-7.

57. Lee CK, Kwak YS, Rhee H, Kim YS, Han JH, Choi JO, et al. The nationwide epidemiological study of mental disorders in Korea. J
Korean Med Sci 1987;2:19-34.

58. Lee CK, Kwak YS, Yamamoto J, Rhee H, Kim YS, Han JH, et al. Psychiatric epidemiology in Korea. Part I: Gender and age
differences in Seoul. J Nerv Ment Dis 1990;178:242-6.

59. Nakamura K, Yamamoto M, Yamazaki O, Kawashima Y, Muto K, Someya T, et al. Prevalence of anorexia nervosa and bulimia
nervosa in a geographically defined area in Japan. Int J Eat Disord 2000;28:173-80.
60. Kuboki T, Nomura S, Ide M, Suematsu H, Araki S. Epidemiological data on anorexia nervosa in Japan. Psychiatry Res 1996;
62:11-6.

61. Azuma Y, Henmi M. A Study on the Incidence of Anorexia Nervosa in Schoolgirls. Annual Report of Research Group in Eating
Disorders; 1982. p. 30-4.

62. Chen CN, Wong J, Lee N, Chan-Ho MW, Lau JT, Fung M. The Shatin community mental health survey in Hong Kong. II. Major
findings. Arch Gen Psychiatry 1993;50:125-33.

63. Nobakht M, Dezhkam M. An epidemiological study of eating disorders in Iran. Int J Eat Disord 2000;28:265-71.

64. Nasser M. Screening for abnormal eating attitudes in a population of Egyptian secondary school girls. Soc Psychiatry Psychiatr
Epidemiol 1994;29:25-30.

65. Mumford DB, Whitehouse AM, Platts M, Choudry I. Survey of eating disorders in English-medium schools in Lahore, Pakistan. Int
J Eat Disord 1992;11:173-84.

66. Lai KY. Anorexia nervosa in Chinese adolescents-does culture make a difference? J Adolesc 2000;23:561-8.

67. Mumford DB, Whitehouse AM. Increased prevalence of bulimia nervosa among Asian schoolgirls. BMJ 1988;297:718.

68. Nasser M. Comparative study of the prevalence of abnormal eating attitudes among Arab female students of both London and
Cairo universities. Psychol Med 1986;16:621-5.

69. DeAngelis T. A genetic link to anorexia. Monit Psychol 2002;33:34-6.

70. Monteleone P, Maj M. Genetic susceptibility to eating disorders: Associated polymorphisms and pharmacogenetic suggestions.
Pharmacogenomics 2008;9:1487-520.

71. Kaye WH, Gwirtsman HE, George DT, Ebert MH. Altered serotonin activity in anorexia nervosa after long-term weight restoration.
Does elevated cerebrospinal fluid 5-hydroxyindoleacetic acid level correlate with rigid and obsessive behavior? Arch Gen Psychiatry
1991;48:556-62.

72. Kaye W. Neurobiology of anorexia and bulimia nervosa. Physiol Behav 2008;94:121-35.

73. Frank GK, Bailer UF, Henry S, Wagner A, Kaye WH. Neuroimaging studies in eating disorders. CNS Spectr 2004;9:539-48.

74. Holliday J, Tchanturia K, Landau S, Collier D, Treasure J. Is impaired set-shifting an endophenotype of anorexia nervosa? Am J
Psychiatry 2005;162:2269-75.

75. Treasure JL. Getting beneath the phenotype of anorexia nervosa: The search for viable endophenotypes and genotypes. Can J
Psychiatry 2007;52:212-9.

76. Lopez C, Tchanturia K, Stahl D, Treasure J. Weak central coherence in eating disorders: A step towards looking for an
endophenotype of eating disorders. J Clin Exp Neuropsychol 2009;31:117-25.

77. Kiriike N, Nagata T, Tanaka M, Nishiwaki S, Takeuchi N, Kawakita Y. Prevalence of binge-eating and bulimia among adolescent
women in Japan. Psychiatry Res 1988;26:163-9.

78. Lee S. Anorexia nervosa in Hong Kong: A Chinese perspective. Psychol Med 1991;21:703-11.

79. Kayano M, Yoshiuchi K, Al-Adawi S, Viernes N, Dorvlo AS, Kumano H, et al. Eating attitudes and body dissatisfaction in
adolescents: Cross-cultural study. Psychiatry Clin Neurosci 2008;62:17-25.

80. Becker AE, Burwell RA, Gilman SE, Herzog DB, Hamburg P. Eating behaviours and attitudes following prolonged exposure to
television among ethnic Fijian adolescent girls. Br J Psychiatry 2002;180:509-14.

81. Mumford DB, Whitehouse AM, Platts M. Sociocultural correlates of eating disorders among Asian schoolgirls in Bradford. Br J
Psychiatry 1991;158:222-8.

82. Vaswani M, Kalra H. Selective serotonin re-uptake inhibitors in anorexia nervosa. Expert Opin Investig Drugs 2004;13:349-57.

83. Powers PS, Santana C. Available pharmacological treatments for anorexia nervosa. Expert Opin Pharmacother 2004;5:2287-92.

84. Jha BK, Awadhia NP. Anorexia nervosa: Review of the syndrome with a case report. Indian J Psychiatry 1967;9:172-80.

85. Neki JS, Mohan D, Sood RK. Anorexia nervosa in a monozygotic twin pair. J Indian Med Assoc 1977;68:98-100.

86. Chadda R, Malhotra S, Asad AG, Bambery P. Socio-cultural factors in anorexia nervosa. Indian J Psychiatry 1987;29:107-11.

87. Mendhekar DN, Arora K, Jiloha RC. Anorexia nervosa with binge eating: A case report. Indian J Psychiatry 2003;45:58-9.

88. Mendhekar DN, Gupta D, Jiloha RC, Baweja A. Atypical bulimia nervosa: A case report. Indian J Psychiatry 2002;44:79-81.

89. Gandhi DH, Appaya MP, Machado T. Anorexia nervosa in Asian children. Br J Psychiatry 1991;159:591-2.

90. Bhugra D, King M. Bulimia nervosa among Asian schoolgirls. BMJ 1988;297:1198.
91. Srinivasan TN, Suresh TR, Jayaram V, Fernandez MP. Eating disorders in India. Indian J Psychiatry 1995;37:26-30.

92. Bhugra D, Bhui K, Gupta KR. Bulimic disorders and sociocentric values in North India. Soc Psychiatry Psychiatr Epidemiol 2000;
35:86-93.

93. Mammen P, Russell S, Russell PS. Prevalence of eating disorders and psychiatric comorbidity among children and adolescents.
Indian Pediatr 2007;44:357-9.

94. Chugh R, Puri S. Affluent adolescent girls of Delhi: Eating and weight concerns. Br J Nutr 2001;86:535-42.

95. Gupta MA, Chaturvedi SK, Chandarana PC, Johnson AM. Weight-related body image concerns among 18-24-year-old women in
Canada and India: An empirical comparative study. J Psychosom Res 2001;50:193-8.

96. Rubin B, Gluck ME, Knoll CM, Lorence M, Geliebter A. Comparison of eating disorders and body image disturbances between
Eastern and Western countries. Eat Weight Disord 2008;13:73-80.

97. Srinivasan TN, Suresh TR, Jayaram V. Emergence of eating disorders in India: Study of eating distress syndrome and
development of a screening questionnaire. Int J Soc Psychiatry 1998;44:189-98.

Pratap. Sharan, A. Sundar

Copyright: COPYRIGHT 2015 Indian Psychiatric Society


http://www.medknow.com
Source Citation (MLA 9th Edition)
Sharan, Pratap, and A. Sundar. "Eating disorders in women." Indian Journal of Psychiatry, vol. 57, no. 6, July 2015, p. 286. Gale
Academic OneFile, link.gale.com/apps/doc/A431997894/AONE?u=j130901&sid=bookmark-AONE&xid=38416f74. Accessed 31
Oct. 2022.
Gale Document Number: GALE|A431997894

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